RT Journal Article
SR Electronic
T1 Edar is a downstream target of beta-catenin and drives collagen accumulation in the mouse prostate
JF Biology Open
JO Biology Open
FD Company of Biologists
SP bio037945
DO 10.1242/bio.037945
VO 8
IS 3
A1 Wegner, Kyle A.
A1 Mehta, Vatsal
A1 Johansson, Jeanette A.
A1 Mueller, Brett R.
A1 Keil, Kimberly P.
A1 Abler, Lisa L.
A1 Marker, Paul C.
A1 Taketo, M. Mark
A1 Headon, Denis J.
A1 Vezina, Chad M.
YR 2019
UL http://bio.biologists.org/content/8/3/bio037945.abstract
AB Beta-catenin (CTNNB1) directs ectodermal appendage spacing by activating ectodysplasin A receptor (EDAR) transcription, but whether CTNNB1 acts by a similar mechanism in the prostate, an endoderm-derived tissue, is unclear. Here we examined the expression, function, and CTNNB1 dependence of the EDAR pathway during prostate development. In situ hybridization studies reveal EDAR pathway components including Wnt10b in the developing prostate and localize these factors to prostatic bud epithelium where CTNNB1 target genes are co-expressed. We used a genetic approach to ectopically activate CTNNB1 in developing mouse prostate and observed focal increases in Edar and Wnt10b mRNAs. We also used a genetic approach to test the prostatic consequences of activating or inhibiting Edar expression. Edar overexpression does not visibly alter prostatic bud formation or branching morphogenesis, and Edar expression is not necessary for either of these events. However, Edar overexpression is associated with an abnormally thick and collagen-rich stroma in adult mouse prostates. These results support CTNNB1 as a transcriptional activator of Edar and Wnt10b in the developing prostate and demonstrate Edar is not only important for ectodermal appendage patterning but also influences collagen organization in adult prostates.This article has an associated First Person interview with the first author of the paper.